Enumeration, functional responses and cytotoxic capacity of MAIT cells in newly diagnosed and relapsed multiple myeloma

NA Gherardin; L Loh; L Admojo; AJ Davenport; K Richardson; A Rogers; PK Darcy; MR Jenkins; HM Prince; SJ Harrison; H Quach; DP Fairlie; K Kedzierska; J McCluskey; AP Uldrich; PJ Neeson; DS Ritchie; DI Godfrey

Journal article

Enumeration, functional responses and cytotoxic capacity of MAIT cells in newly diagnosed and relapsed multiple myeloma

NA Gherardin, L Loh, L Admojo, AJ Davenport, K Richardson, A Rogers, PK Darcy, MR Jenkins, HM Prince, SJ Harrison, H Quach, DP Fairlie, K Kedzierska, J McCluskey, AP Uldrich, PJ Neeson, DS Ritchie, DI Godfrey

Scientific Reports | NATURE PORTFOLIO | Published : 2018

DOI: 10.1038/s41598-018-22130-1

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Abstract

Mucosal-associated invariant T (MAIT) cells are T cells that recognise vitamin-B derivative Ag presented by the MHC-related-protein 1 (MR1) antigen-presenting molecule. While MAIT cells are highly abundant in humans, their role in tumour immunity remains unknown. Here we have analysed the frequency and function of MAIT cells in multiple myeloma (MM) patients. We show that MAIT cell frequency in blood is reduced compared to healthy adult donors, but comparable to elderly healthy control donors. Furthermore, there was no evidence that MAIT cells accumulated at the disease site (bone marrow) of these patients. Newly diagnosed MM patient MAIT cells had reduced IFNγ production and CD27 expression..

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University of Melbourne Researchers

Nicholas Gherardin Author

Liyen Loh Author

Misty Jenkins Author

Henry Prince Author

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Grants

Awarded by Australian Respiratory Council

Funding Acknowledgements

We thank staff from the Flow Cytometry facility at the Department of Microbiology and Immunology at The University of Melbourne. This work was supported by the National Health and Medical Research Council of Australia (NHMRC) under grants 1013667, 1113293 and 1063587, and the Australian Research Council (ARC) under grants CE140100011 and LE110100106. N.A.G. was supported by a Leukaemia Foundation of Australia Postgraduate Scholarship and a Cancer Council Victoria Postdoctoral Fellowship; M.R.J. is supported by an NHMRC Project Grant and fellowship. P.K.D. is supported by an NHMRC Senior Research Fellowship (1041828, 1136680). A.P.U. is supported by an ARC Future Fellowship (FT140100278); K. K. is supported by an NHMRC Senior Research Fellowship (1102792); D.P.F. and D.I.G. are supported by NHMRC Senior Principal Research Fellowships (1117017, 1020770 and 1117766).